Atrioventricular block

Atrioventricular block (AV block) is characterized by an interrupted or delayed conduction between the atria and the ventricles. There are three degrees of AV block, categorized according to the extent of the delay or interruption. First-degree blocks are identifiable on ECG by a prolonged PR interval. Second-degree AV blocks are further divided into four subtypes: Mobitz type I (also called Wenckebach), Mobitz type II, 2:1 AV block, and high-grade AV block. In Mobitz type I blocks, a progressive prolongation of the PR interval culminates in a nonconducted P wave (“dropped beat”). Mobitz type II blocks generate dropped QRS complexes at regular intervals (e.g., 3:2, 4:3, or 5:4), often leading to bradycardia. A 2:1 AV block has a regular pattern in which every second atrial impulse is not conducted to the ventricles. In second-degree high-grade AV block, two or more consecutive P waves do not generate a ventricular response. A third-degree AV block, also known as complete heart block, involves the total interruption of the electrical impulse between the atria and ventricles. The complete absence of conduction results in a ventricular escape rhythm, whose rate depends on the level at which the escape rhythm is generated. AV blocks may be asymptomatic or cause symptoms of bradycardia. Depending on the heart rate, symptoms can be severe and include heart failure or syncope. Asymptomatic patients with first-degree and Mobitz type I blocks usually only require observation, whereas higher-degree blocks necessitate permanent pacemaker insertion.

See “Management approach to patients with AV block” for more information on investigations, monitoring, definitive treatment, and stabilization of unstable bradycardia.

See also “Causes of bradycardia.”

• AV blocks result from the interruption of the electrical impulse anywhere within the atrioventricular conduction system, including the:
  • AV node
  • Bundle of His
  • Left and right bundle branches
• Blocks at the level of the AV node: impulse passes through AV node → normal propagation through conduction system → narrow QRS complex
• Infranodal block
  • Can be at the level of OR below the bundle of His
  • Ventricular depolarization is impeded → wide QRS complex
• More distal AV blocks: typically result from more extensive damage to the conducting system → ↑ risk of progression to complete heart block. ^[8]

• Asymptomatic (common): especially with first-degree and Mobitz type I blocks ^[2]
• Clinical features of end-organ hypoperfusion (due to bradycardia) may be present, including: ^[9]
  • Fatigue
  • Exercise intolerance
  • Dyspnea
  • Dizziness
  • Syncope
• Irregular rhythms (e.g., Mobitz I): palpitations
• Loss of atrioventricular synchrony (e.g., extreme 1° AV block or 3° AV block) : ^[2]
  • Feeling of pulsations in the neck or chest
  • Cannon A waves: physical examination finding seen in AV dissociation (e.g., in third-degree heart block)
    • Caused by the atria and ventricles contracting simultaneously, which leads to blood being pushed against a closed tricuspid valve
    • The result is a retrograde pressure wave throughout the venous system that may appear as pulsations in the jugular vein.
  • Symptoms of heart failure ^[2]
• Significant pauses of asystole
  • Stokes-Adams attacks ^[10]
    • Sudden losses of consciousness that may occur with brief prodromal symptoms, e.g., dizziness, or without any warning, usually lasting a few seconds
    • Attacks are caused by ventricular asystole, most commonly due to third-degree heart block, especially idiopathic paroxysmal AV block.
  • Cardiac arrest

• Description ^[2]
  • PR interval > 200 ms
  • No interruption in atrial to ventricular conduction
  • Rate of SA node = heart rate
  • Often discovered incidentally on ECG
• Risk of progression to complete heart block: low, as the block results from slowed conduction through the AV node ^[2]

Mobitz type I (Wenckebach) ^[2]

• Description
  • Progressive lengthening of the PR interval until a beat is dropped, which means a regular atrial impulse does not reach the ventricles (a normal P wave is not followed by a QRS complex)
  • Mostly regular rhythm separated by short pauses, which may lead to bradycardia (regularly irregular rhythm)
  • Rate of SA node > heart rate
• Risk of progression to complete heart block: typically low, as the block is most often at the level of the AV node

First-degree and Mobitz type I second-degree AV blocks may be seen in healthy individuals, e.g., in athletes with increased vagal tone. Patients are often asymptomatic.

Mobitz type II ^[2]

• Description
  • Single or intermittent nonconducted P waves without QRS complexes
  • The PR interval remains constant.
  • The conduction of atrial impulses to the ventricles typically follows a regular pattern, e.g.: ^[2]
    • 3:2 block: regular AV block with 3 atrial depolarizations but only 2 atrial impulses that reach the ventricles (heart rate = ⅔ SA node rate)
    • 4:3 block: regular AV block with 4 atrial depolarizations but only 3 atrial impulses that reach the ventricles (heart rate = ¾ SA node rate)
  • While 2:1 block follows a regular pattern, it cannot be classified as Mobitz type I or II and is classified separately (see “2:1 AV block”). ^[2]
• Risk of progression to complete heart block: high (> 50%), as it is typically due to infranodal block (usually in the His-Purkinje system) ^[7]

Mobitz type II block can progress to third-degree heart block; therefore, all patients should be admitted for continuous cardiac monitoring and treatment.

Other variants

2:1 AV block ^[2]

• Description
  • Inhibited conduction of every second atrial depolarization (P wave) to the ventricles (heart rate = ½ SA node rate)
  • Cannot be classified as Mobitz I or Mobitz II as only one PR interval is observed before the subsequent dropped complex
  • Often a transient rhythm occurring on a baseline Mobitz I or Mobitz II rhythm
• Risk of progression to complete heart block: depends on level of block
  • Block at the level of the AV node (more common): low
  • Infranodal block (less common): high

High-grade AV block ^[2][7]

• Description
  • A block in which ≥ 2 consecutive P waves do not generate a ventricular response, e.g., 3:1 block
  • As some P waves do generate a ventricular response, high-grade AV block differs from third-degree heart block in which there is complete dissociation.
• Risk of progression to complete heart block: typically high, but depends on duration and reversibility of block

• Description
  • Third-degree AV block is a complete block with no conduction between the atria and ventricles.
  • P waves and QRS complexes have their own regular rhythm but bear no relationship to each other (AV dissociation).
• Risk of progression to cardiogenic shock or cardiac arrest: : High; Sudden onset 3° AV block can result in ventricular asystole, which lasts until an escape rhythm takes over.
• Escape rhythms: can be generated by sites that are usually located near the AV node or near the bundle of His.
  • Ventricular escape rhythm ^[11]
    • A rhythm generated at the level of the bundle of His
    • Heart rate 20–40/minute
    • Wide QRS complexes
  • Junctional escape rhythm ^[11]
    • A rhythm generated at the level of the AV node
    • Heart rate 40–60/minute
    • Narrow QRS complexes
• Idiopathic paroxysmal AV block ^[12]
  • A subtype of third-degree AV block that can affect patients with otherwise normal AV conduction.
  • Recurrent episodes may lead to Stokes-Adams attacks.

• Left bundle branch block
• Right bundle branch block
• Left anterior fascicular block
• Left posterior fascicular block
• Sinus node dysfunction
• See also “Causes of bradycardia.”

The differential diagnoses listed here are not exhaustive.

Approach

• All patients
  • Obtain 12-lead ECG immediately (with or without rhythm strip) to ascertain the type of AV block.
  • Evaluate for signs of unstable bradycardia and apply transcutaneous pacing pads if required.

Evaluation of underlying causes ^[2][13]

• Order laboratory studies based on suspected etiology, e.g.:
  • Renal function tests
  • Liver chemistries
  • Troponin
  • Antibody titer, e.g. for Lyme disease
  • Electrolytes (including potassium)
  • Blood gas (serum pH)
  • TSH
• Identify medications that can impair AV conduction.
  • Beta-blockers
  • Non-dihydropyridine calcium channel blockers
  • Digoxin
  • Others: clonidine, amiodarone, adenosine, flecainide, class IB antiarrhythmics, and some antidepressants.
• Consider measuring drug levels: e.g. digoxin level

Management of low-risk AV block ^[2]

• Patients on medication that can cause or exacerbate AV conduction
  • Monitor for progression with periodic ECGs.
  • Discontinue if patients have other preexisting conduction abnormalities. ^[13]

Indications for pacemaker placement ^[2]

Patients with an irreversible AV block and the following:

• Infranodal block
  • Patients with infranodal block should be treated as high-grade AV blocks
  • If the level of the AV block is unclear, assess with ^[2][7]
    • Exercise ECG
    • Electrophysiologic study
    • Carotid sinus massage or pharmacological challenge
• Neuromuscular disease associated with AV block (known or suspected): refer to a specialist for possible pacemaker.
• Certain symptomatic patients
  • Assess for correlation of symptoms using an ambulatory Holter monitor.
    • Permanent pacing is indicated if symptoms clearly correlate with AV block.
    • If symptoms do not correlate, continue monitoring as an outpatient

Management of high-risk AV block ^[2][13]

• Potentially reversible cause
  • Consider temporary pacing.
  • Adapt management depending on the suspected underlying cause
    • Discontinue or reduce medications causing AV block or follow detoxification strategies in case of:
      • Beta blocker toxicity
      • Digoxin toxicity
      • CCB toxicity
    • Perform PCI and avoid early pacemaker implantation < 72 h in patients with AV block caused by acute MI.
    • See “Special considerations” in “Symptomatic, stable bradycardia” for further detail.
  • Permanent pacemaker placement is indicated if:
    • AV block persists despite adequate treatment
    • Medication causing AV block is necessary and not replaceable
• Irreversible cause
  • All patients with Mobitz Type II, high-grade, or third-degree AV block require the placement of a permanent pacemaker.
  • Consider a defibrillator if the AV block is caused by infiltrative processes or neuromuscular disease with conduction block.

All patients

• Review ECG.
• Evaluate for signs of end-organ hypoperfusion and apply transcutaneous pacing pads as needed.
• Admit with continuous cardiac monitoring: complete heart block, Mobitz II, or high-grade AV block.
• Can investigate as an outpatient unless hemodynamically unstable: 1° AV block, 2:1 heart block, or Mobitz I
• Identify and treat underlying causes.

Hemodynamically unstable patients (see “Unstable bradycardia”)

• Consider atropine with or without beta agonists. ^[2]
• Begin temporary cardiac pacing.
• Plan permanent pacemaker placement (with or without defibrillator) if cause is nonreversible.

Hemodynamically stable patients

• Consider assessment for pacemaker indications in patients with low-risk AV blocks.
  • Ambulatory Holter ECG in symptomatic patients to ensure the arrhythmia correlates with symptoms
  • Carotid sinus massage, exercise ECG, or EPS to assess level of the AV block
• Plan permanent pacemaker placement (with or without defibrillator) in patients with:
  • High-risk AV block (Mobitz II, high-grade AV block, 3° AV block)
  • Low-risk AV block and:
    • Symptoms that correlate with the block
    • Neuromuscular disease
    • Infranodal block